Shock

If the patient is chronically in atrial fib, the shock rarely works. Your patient is unstable, so you decide to give it a shot. You might as well give yourself the best chance of success, so go right for 360 J on monophasic, or equivalently high on your biphasic. This will not cause more injury than lower joules (Heart 1998, 80:3 and Resuscitation 1998;36:193). PA is probably better than AA if you have pads. Make sure the synch is on.

You need to give your patient something to disguise the fact that you are electrocuting them. Yet you don’t want to drop their pressure. Ketamine is ok in disassociative dosing, but then your patient is loopy and you lose your mental status exam. Consider 5-7 mg of etomidate along with a pain dose of ketamine, 10-15 mg.

Screen for WPW

If you have a. fib with a wide QRS and a rate > 250-300, be scared, very scared. This is WPW and these patients just love to ruin your day by going into v. fib. Shock early, shock often, light them up.

Get the BP Up

So you made sure it’s not WPW and the cardioversion has failed, as it so often does in chronic a. fib. Now you need to raise the BP before anything else. Use push-dose phenylephrine. 50-200 mcg every minute or so until you get the blood pressure above a diastolic of 60; this will temporize the situation and make the patient’s heart more likely to slow down.

Though things look better, you have not really fixed the problem, you have just temporized.

Slow them them down

Give either amiodarone 150 mg bolus and then the drip (may repeat the bolus x 1)

Or

Use diltiazem, but not as a push. Drip it in at 2.5 mg/minute until HR < 100 or you get to 50 mg. (Resuscitation 52:167, 2002) See here for more.

Still not working?

Consider magnesium

Consider reshocking

Consider cardiology consult

Consider something else is going on

Consider signing out to one of your colleagues and running away

Update:

This study would indicate that perhaps we are doing more harm than good when we aggressively try to control rate or rhythm in stable (non-crashing) patients (Ann Emerg Med 2015;65(5):511)

Would you prefer metoprolol for rapid afib if the pt is already on it?

For years, I’ve been encouraged to avoid using more than one class of AV blocking agents at a time if avoidable. Most chronic Afib pts come in on metoprolol, sometimes in addition to another agent (e.g. Digoxin). I have the most experience with diltiazem for treating rapid afib, but would it make sense to start with metoprolol for this patient, as we may avoid combining agents to increase the chance of causing complete heart block? It seems like the ED usually prefers dilt, while cardiology often prefers metoprolol.
P.S. What about procainamide for unstable Afib with WPW?
Thanks.

I wouldn’t consider the patient’s home meds to contraindicate your choice in the ED. I think the way to go is to avoid giving two classes of meds IV. Procainamide is just built to lower the pt’s BP, so even with phenylephrine, I think you are better off avoiding it in a hypotensive patient. But if they are not shocking out, you can consider it.

Great talk about a scary topic.
In Australia, instead of phenylephrine, Metaraminol (Aramine) is a more popular drug, It is a fast acting peripheral vasocontrictor, loved by most anesthetist. In common practice, most doctors would mix one ampoule (2 mg) with Normal Saline to make up 20 ml and give one to two ml at a time. The bolus dose of Amiodaro0ne recommended is 3oomg followed by an infusion. I came across a similar case of crashing AF > 170 and hypotension 70/50 not long ago. To make the situation worse, he had infective COPD /type 2 respiratory failure with a high pCO2 of 85. Fortunately, the emergent cardioversion worked and he improved on NIV.

Thanks for the info and the comment. It sounds like metaraminol is very similar to phenylephrine. So you folks start with the higher dose of amio right off the bat? Do you see a lot of hypotension from it?

I ve read about the use of calcium as a pre treatment agent prior the use of calcium channel blockers ie ditialzem. They advocated us to give 5-10cc of calcium gluconate as to offset the hypotensive effect of the drug.
What do you think?

Calcium showed good effect as a pretreatment for verapamil. The data have not supported Ca pretreatment for dilt (J Emerg Med. 2004 May;26(4):395-400). However even though this study was an RCT, it was fairly useless b/c almost none of the patients got hypotensive in either group. However, calcium is an excellent inopressor in any patient, so I heartily agree that it would be a great thing to give in the patient above. Thanks for the comment.

nice lecture, pharmacist guy is learning alot, amio and diltiazem is very good for rate control, question why Phenyleph of all the pressors, u just want pure alpha effect and nothing to accelerate an already 250-300 HR?

Hey Scott,
Great podcast. I heard the “gray hairs” in my dept talk about Dig, but it takes forever to kick in, right? Any role for it acutely, EVER?
Another obscure but cool-sounding strategy I have actually done a few times is to pretreat with CaGluconate then give small (5mg) Diltiazem boluses. Taught to me by said gray-hairs, this has little evidence. There was a small RCT in JEM 2004 that showed no difference in hypotension with Calcium vs. Placebo in RVR patients (J Emerg Med. 2004 May;26(4):395-400).
Have you done this?

Hi Scott. NICE talk on the Crashing AFib patient – which I’m only getting to in 2012 … (you first recorded this in 2010 … ).

As per above few comments – Calcium pre-treatment seems an option (realizing as you mention the data is with Verapamil) – but I believe YOUR emphasis in your podcast of using lower doses of IV Dilt given slower is the REAL key. Doing so has got to minimize the hypotensive effect. Clearly there is a balance one is seeking – which is to slow the rate of AFib (so as to increase diastolic filling time and improve hemodynamics) while not giving IV Dilt at too fast a rate such that BP is further lowered …. BP will come up IF you can improve LV filling and cardiac output – and the “art” is trying to balance the two …

As to Dig – my training says different than the textbooks (I completed my residency in 1975-1978) – so Dig is a drug that I’ve had a LOT of experience with during my earlier years of practice. I used it ALL the time in new-onset AFib. I fully agree with you – that IV Diltiazem is clearly preferred for initial new-onset rapid AFib (vs perhaps an IV beta-blocker in several select instances when increased sympathetic tone is felt to be operative) – but my point is that Dig will OFTEN begin to work within 15-20 minutes IF you bolus the patient (which is safe is the patient is not on the drug). Dig clearly has the advantage of being the ONLY agent among those used that increases inotropy (albeit by a limited amount), and doesn’t lower BP.

I realize in 2012 that the days of loading patients with IV Dig are pretty much GONE (and given unfamiliarity of currently-trained providers with the Drug, this may be best … ) – but my point is that this drug WILL often work much sooner than “in a few hours” if it is administered the way it used to commonly be used.

Absolutely agree. I love digoxin for the “nearly crashing” patient, and even if the peak effect may take hours, you get 80-90% effect in most patients in 15-30minutes, which, depending on the scenario, may be perfectly fine. And of course, no hypotension…

I agree with the use of digoxin in these situations. I presume it is inexpensive, and it does seem to kick in within fifteen minutes or so. I start with 0.25 mg and never had to go beyond a total of 0.5 mg. Digoxin is an example of “an oldie, but goodie.”

ROB – I’ll qualify my response by advising that I retired from my faculty slot in July, 2010 (after 30 years). I’m now “Emeritus” (which means I’m no longer practicing) – but the dosing I used for many years when practicing (and attending) regarding use of Digoxin is as follows:

– IF the patient has not previously been on the drug – consider IV loading (with 0.25-0.5 mg as the initial dose).
– May follow this with smaller IV increments (of 0.125-0.25 mg) every 2-6 hours, until a total loading dose (0f ~0.75-1.5mg) has been given over the first 24 hours. I’d use the lower range (~0.75 mg) for my loading dose with older patients, those with renal disease, those who are frail.
– In years past before my time, higher doses (of 0.5-0.75 mg) were given for initial IV loading. I always preferred use of lower boluses (as above) – which I felt was safer. I’d then be able to repeat smaller IV increments every 2-6 hours as above.
– The effect of Dig for a patient in rapid AFib may be synergistic with other agents (ie, with smaller doses of Dilt or beta-blockers) – it is a “1 + 1 = 5” effect.
– Although full effect of Dig might not be for hours – I found rate slowing sometimes occurring within the first 15-30 minutes.
– The next day (after completion of IV loading) – the daily oral maintenance dose may be started. For most patients under ~60 yo (assuming they have normal renal function) – the daily oral maintenance dose = 0.25 mg/day.
– Lower doses should be used for older patients and/or those with renal impairment (0.125 mg PO – or even 0.125mg every other day).
– Dig is not totally absorbed when given PO. It is ~2/3 absorbed – so that an IV dose of 0.25 mg corresponds to a higher dose of the drug given orally.
– The “30-second” pharmacokinetics to be aware of is that the half-life of Dig is between 36 hours (in a healthy young adult) and ~5 days (in an older patient with renal failure). You can guesstimate what the half-life will be for your patient based on these 2 end points (Knowing the half-life is helpful if your patient gets toxic – since it gives you an idea for how long the drug will hang around).

Hi Scott! I’m revisiting this post (as I revisit many of your “classics”) for a refresher and for the first time noticed the recommendation for ketamine during cardioversion. I’ve switched to ketamine or ketamine/propofol for most of my ED sedation needs at this point, but given its propensity for causing tachycardia in otherwise healthy people I wonder if there is any theoretical or practical concern about exacerbating a tachydysrhythmia with it.

On an unrelated but amusing note I used ketamine/propofol for a semi-elective cardioversion recently and had the closest thing to an emergence reaction I’ve ever seen where the poor guy woke up repeating “I died I died I died I died, am I dead?” for over an hour with his wife at the bedside wondering what the hell we did to him. He would potentially have benefited from a benzo in hindsight …

Anyway, if you have any insight on the tachycardia issue I’d be interested to hear it. As ketamine isn’t really in the “mainstream” sedation algorithm for middle aged to older folks in rapid afib I would prefer to avoid any adverse outcomes from it.

I had recent case of a late 40s, relatively healthy man who presented with shortness of breath. He was in a rapid SVT (probably a fib) with a rate of 190 and systolic BP in the 60s in the field and was cardioverted without sedation to sinus rhythm. SBP improved to 80s. When I saw him he was in sinus tach in the 110s, SBP 70s-80s. CXR showed dense right middle and lower lobe infiltrates. He was aggressively fluid resuscitated and BP temporarily improved, but then he went back into a fib with a rate in the 180s-200s. He was severely symptomatic complaining of chest pain, appeared to be worsening, and SBP was back in the 60s. Since cardioversion had worked in the field I figured it was worth a try. I gave 0.25mg/kg of ketamine and attempted cardioversion at 200 biphasic J twice without success. I then started amiodarone. The patient was obviously in septic shock which was the reason for his tachycardia and hyperadrenergic state. But I couldn’t help wondering if ketamine was a poor choice on my part. Other sedatives all would have presented problems in this case. I suppose etomidate had the least downside but it depends on where you stand on the adrenal suppression in sepsis debate. The patient converted on the amio drip several hours after transfer to the ICU.

I did a brief lit search and there doesn’t seem to be much on ketamine in these situations.

Julie’s comment led me to relisten to this podcast – which gave me 2 additional thoughts I wanted to comment on re the ‘Crashing AFib Patient’:

The rate of AFib doesn’t have to be 300/minute for me to begin thinking about WPW. Rapid AFib with a wide QRS over 220/minute is enough to start one thinking. An interesting accompaniment of very rapid AFib with WPW is that there will often be marked variation in the length of the R-R interval (some relatively long R-R interval intermixed with much shorter ones). For a nice illustrative case – GO TO: http://ecg-interpretation.blogspot.com/2012/02/ecg-interpretation-review-37-irregular.html /

As to rapid AFib with hypotension (but no WPW) rarely responding to electrical cardioversion – a lot depends on the reason on the reason for new-onset AFib. One KEY to management will be identifying and fixing the precipitating cause of the AFib (be it new heart failure, hypovolemia, etc.).

While using amiodarone for a crashing a-fib patient, is there any concern that although the patient does not have the typical HR associated with WPW, that there is an accessory pathway? Amiodarone does have BB and calcium channel effects that can block AV nodal conduction and therefore leave the heart susceptible to v-fib by allowing conduction to travel freely through the accessory channel. Is there any harm in using procainamide as the first line antiarrythmic in this scenario?
Thank

It only matters if the patient is demonstrating antidromic conduction. Known WPW, sure don’t use amio. But in a patient with unknown WPW, but with a narrow QRS and a rate <200, I would not worry about it. Wide, fast, and A-Fib--give procainamide or shock them.

How long would you typically observe a elderly patient after administering a 150 mg bolus of amiodrone with the drip to follow. We recently had a patient 5 days post CABG who went into a-fib with long pauses of 7 to 8 seconds.

For us prehospital folks without access to lots of pressors…any consideration for starting a dopamine drip at alpha-dominant doses? Or is there enough beta-blocking activity, even at 15-20 mikes, to speed the rate up further and defeat the purpose?

Thanks for the great podcast . What about norepinephrine which has mainly alpha stimulant effect so little change in heart rate can it be used instead of norepinephrine? What do you think?
Can we use midazolam for sedation in the shocked patient and would it be enough for cardioverting the shocked patient?…thank alot for your kindness

I had trouble deciding what to do recently on a patient who presented with decompensated CHF and rapid a fib. The cardioversion worked, but his pressure remained in the 70’s in NSR afterwards, with signs of poor perfusion. I thought about push dose phenyl, but second guessed myself because I didn’t want to worsen the afterload on an LVEF that was previously documented around 30%, maybe making perfusion worse. Thought about + inotropes, but didn’t want to worsen ischemia or revert back to rapid a fib. I ended up calling cardiology and they scratched their heads for about 30 minutes and then started levo. Pressures eventually normalized and he recovered back to baseline in a few days. Any thoughts?

the ? is easier for whom? It is sharply frowned upon to withdraw fluid from the bag before adding medications b/c it adds to complexity of mixing, leads to more likelihood of breaks in sterility, and more potential for mishaps. Even if you made a nice 1mg/ml drip, managing the infusion rates and dosing without a drip sheet is just setting yourself up for error. With a drip sheet, it doesn’t matter what the concentration is, because you are just following the sheet.

What are your thoughts on the use of procainamide for the acute, non-crashing AFib patient? US and European guidelines cite a lack of evidence for their non-promotion of it. There was a recent study out of Canada promoting it, and we have a couple doctors here that seem to go after it as their first choice, and it makes me, as a pharmacist, a little uneasy.

Scott,
Had a few crashing A-Fib pts of late. I used Esmolol in both cases. Revisited this cast. Surprised Esmolol specifically not mentioned here. What is your gen experience and take on Esmolol for the crashing A-Fib pt?

I’d like to thank you for the great work you’re doing, I have learnt really a lot from your podcasts and some times when I’m in doubt what to do I ask myself WWWD (what would Weingart do) and it always helps.

A while ago I had a 60 yr old patient with a history of MI 6 month ago with monomorphic VT 220 bpm, his SBP was around 60, he was still conscious, we cardioverted him … would you chose the same sedation/analgesia (ethomidate + ketamine) agents as you have mentioned in this podcast? In one book of EM cases it says they only recommend Fentanyl 100 – 200 mcg because it should have the least negative inotropic effect, what do you think about that? What do you think of phenylephrine before using sedation agents in this case?
Well at the end the cardioversion was successful in restoring SR and the patient also fell better:)

Regarding hypotensive patients with Atrial fibrillation in RVR, Ive had some success with a combination of digoxin 0.5mg IV and a Dobutamine drip. I tend to shy away from dopamine since it too can increase the heart rate.

Scott, I’m a medic – what if I’m in the field – and cardioversion fails, and I do not have push-dose phenylephrine? This was nearly the case recently (transfer of very unstable a-fib RVR patient, hypotensive, but the patient crashed just before we got there, and thus the transfer was cancelled). My service carries Epi and Dopamine.

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Hi, my name is Scott Weingart. I am an ED
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